Chemical modification of the protein eukaryotic elongation factor 1A1 (eEF1A1) regulates remyelination, a new study suggests, indicating that the processes regulating this protein may provide useful therapeutic targets for multiple sclerosis (MS).
The study, “EEF1A1 deacetylation enables transcriptional activation of remyelination,” was published in Nature Communications.
Myelin is a “sheath” of protein and fat molecules that wraps around neurons and is critical for proper neuronal function. MS and some other neurological conditions are characterized by a loss of myelin. Restoring lost myelin — termed remyelination — is a goal of MS research.
The nervous system can be broadly divided into two parts: the central nervous system (CNS), consisting of the brain and spinal cord, and the peripheral nervous system (PNS), which encompasses everything else. When neuronal damage occurs, remyelination can occur in the PNS, but in the CNS it is more limited and less efficient for reasons that are not fully understood.
“In order to promote the restoration of myelin, we need to understand the process that controls the mechanism,” Claire Jacob, co-author of the study and professor at Johannes Gutenberg University Mainz in Germany, said in a press release.
SOX10 is a transcription factor — a protein responsible for controlling gene expression (the extent to which different genes are turned “off” or “on”). When SOX10 is active, it promotes the activity of genes linked to remyelination. However, the factors that regulate SOX10 itself have not been fully elucidated.
Previous research showed that two related proteins, HDAC1 and HDAC2, are necessary for SOX10 function. These proteins regulate acetylation — a type of chemical modification involving the addition of an acetyl group, which can regulate protein function.
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